44: Infections Acquired in the Intensive Care Unit


CHAPTER 44
Infections Acquired in the Intensive Care Unit


James S. Salonia1 and Andre Sotelo2


1 Icahn School of Medicine at Mount Sinai, New York, NY, USA


2 Hackensack University Medical Center, Hackensack, NJ, USA


General treatment rationale



  • When an ICU‐acquired infection is suspected, all devices should be removed when possible.
  • Antimicrobial agents are the primary treatment. These antibiotics should be administered promptly, as a delay in treatment may lead to increased mortality.
  • Choice of specific antibiotic agents should be determined by risk factors, local microbiology, and hospital‐based antibiograms.
  • Initial therapy should be administered intravenously with a transition to oral therapy in patients with appropriate clinical response. For C. difficile infection, oral treatment is preferred when possible.

General prevention



  • Hand hygiene (conventional soap and water or alcohol‐based hand sanitizer) and aseptic technique (maximal sterile barrier precautions with cap, mask, sterile gown, gloves, and full body drape).
  • Implementation of quality improvement programs and daily assessment of bundle adherence measures for all intravascular devices, indwelling urinary catheters, and endotracheal tubes.
  • All patients with suspected or laboratory confirmed C. difficile infections should be placed on contact precautions, utilizing barrier protection with gown, gloves, and disposable instruments (e.g. stethoscope). Hand hygiene with conventional soap and water is critical, as alcohol‐based hand rubs do not prevent the spread of C. difficile spores.
  • Simulation‐based training can be an effective tool to instruct health care providers in the proper technique of utilizing maximal sterile barrier precautions and on the proper placement of intravascular catheters and endotracheal intubation.

Central line‐associated bloodstream infections


Background


Definition of disease



  • CLABSI is a laboratory confirmed bloodstream infection where a central line was in place for >2 calendar days on the date of event, with the day of device placement designated as day 1. If the central line was in place for >2 calendar days and then removed, the date of laboratory confirmed bloodstream infection must be the day of discontinuation or the following day.

Etiology


Predominant organisms are:



  • Coagulase‐negative staphylococci.
  • Staphylococcus aureus.
  • Candida species.
  • Enteric Gram‐negative bacilli.

Pathology/pathogenesis



  • Pathogenic microbes are introduced through migration of skin organisms at the insertion site into the cutaneous catheter tract and along the surface of the catheter, with colonization of the catheter tip. This is the most common route of infection for short‐term catheters.
  • Direct contamination of the catheter or catheter hub, contact with hands or contaminated fluids or devices, hematogenously seeded infection from another focus of infection, and infusate contamination are less common methods of colonization and infection.

Predictive/risk factors



  • Prolonged central venous or arterial catheterization.
  • Skill of the operator.
  • Insertion site risk factors:

    • Chlorhexidine‐based solutions preferred.
    • Loss of skin integrity (e.g. burns, psoriasis).

  • Submaximal barrier precautions.
  • Non‐tunneled greater than tunneled catheters.
  • Type of catheter:

    • Number of lumens.
    • Lower risk with antibiotic impregnated catheters.
    • Greatest risk with pulmonary artery catheters.

  • Repeated catheterization and use.
  • Catheter site:

    • Femoral site has highest risk of infection.
    • Pre‐existing infection overlying insertion site.

  • Insertion circumstance:

    • Emergency greater than elective.

  • Severity of illness, chronic illness, and immune deficient state:

    • Granulocytopenia.
    • Immunosuppressive chemotherapy.

  • Total parenteral nutrition (TPN) administration.

Prevention



  • Utilize and maintain maximal sterile barrier precautions when inserting intravascular catheters.
  • Insertion site preparation:

    • 2% chlorhexidine‐based solutions preferred.
    • Alternatives include iodine‐based solutions.

  • A subclavian or jugular site is the preferred location for central venous catheter placement. Avoid using the femoral vein for central venous access.
  • The use of antiseptic/antibiotic impregnated short‐term central venous catheters and chlorhexidine impregnated sponge dressings is recommended if the rate of infection is not decreasing despite adherence to other strategies.
  • Catheter stabilization with a sutureless securement device is preferred to avoid disruption around the catheter entry site.
  • If catheter site is bleeding or oozing, the use of sterile gauze is recommended until bleeding has resolved.
  • Prompt removal of intravascular catheter when no longer indicated.

Diagnosis


Typical presentation



  • Unexplained fever, leukocytosis, and decompensation in a patient with central venous or arterial access.
  • Erythema, induration, and tenderness at the insertion site.

Clinical diagnosis


History

Prolonged intravascular catheterization in the presence of symptoms such as fever, chills, and rigors should increase suspicion for a catheter‐associated bloodstream infection.


Physical examination

Daily examination of all catheter insertion sites for erythema, purulent discharge, and tenderness.


Laboratory diagnosis


List of diagnostic tests


  • Paired aerobic and anaerobic blood cultures (at least one culture set from a peripheral vein), are collected in a sterile manner prior to the initiation of antibiotics. Skin preparation should be performed utilizing chlorhexidine.
  • Quantitative catheter tip cultures have been utilized for diagnosis of CLABSI, using growth of >15 colony forming units (cfu) as positive. A positive catheter tip culture itself, however, is not sufficient for diagnosis.

List of imaging techniques


  • Echocardiogram may be necessary in patients with CLABSI to evaluate for infective endocarditis.

Potential pitfalls/common errors made regarding diagnosis of disease



  • Failure to implement or adhere to central line insertion checklist or full compliance with central line maintenance bundle adherence measures.
  • Lack of aseptic technique in the collection of blood cultures may result in contamination and false positive cultures.

Treatment



  • Duration of antibiotic therapy is dependent on pathogenic organism. Duration of antibiotics is counted from the first day of negative blood cultures.
  • Vancomycin is recommended for empiric therapy due to prevalence of MRSA.
  • Empiric coverage for Gram‐negative organisms is recommended until cultures are available.
  • Empiric coverage for multidrug‐resistant (MDR) organisms is recommended for select patients:

    • Neutropenic patients.
    • Severely ill patients.
    • Known colonization with MDR pathogens.

  • Empiric coverage for Candida species with echinocandin may be recommended for patients with certain risk factors:

    • Total parenteral nutrition.
    • Prolonged duration of broad spectrum antibiotics.
    • Hematologic malignancy.
    • Transplant recipient.
    • Colonization due to Candida species.

  • Catheterized patients with a single positive blood culture growing coagulase‐negative Staphylococcus species may have additional cultures collected prior to considering catheter removal.

Prognosis


Mortality from CLABSI is approximately 12–25% and is influenced by the underlying acute illness and comorbidities.


Follow‐up tests and monitoring



  • Patients with CLABSI require close follow‐up with surveillance blood cultures to demonstrate clearance of bacteremia.
  • Persistent bacteremia and/or persistent symptoms 72 hours after catheter removal with appropriate antibiotics suggest complications such as infective endocarditis and/or metastatic infections.

Catheter‐associated urinary tract infections


Background


Definition of disease



  • CAUTI:

    • Laboratory confirmed infection where an indwelling urinary catheter was in place for >2 calendar days on the date of event, with the day of device placement designated as day 1 and was still present on or removed the day prior to the date of event and the patient has at least one of the following signs or symptoms:

      • Fever (>38°C).
      • Urinary urgency or frequency.
      • Dysuria.
      • Suprapubic or costovertebral pain or tenderness.
      • Altered metal status.

    • Plus, positive urine culture with no more than two species of organisms with at least one species of >100 000 cfu.

Incidence/prevalence



  • CAUTI is the most common healthcare‐associated infection.

Etiology



  • Predominant organisms are:

    • Escherichia coli.
    • Enterococcus.
    • Candida species.
    • Klebsiella species.
    • Pseudomonas aeruginosa.
    • Serratia species.
    • Citrobacter species.
    • Enterobacter species.

Long‐term catheterization usually results in polymicrobial infections.


Pathology/pathogenesis



  • Introduction of pathogenic microbes into the urinary system as a result of improper sterile technique with catheter placement, prolonged catheter insertion with migration of meatal, vaginal, or rectal microorganisms forming biofilms on the foreign catheter, and failure to maintain a closed drainage system are the most important mechanisms of CAUTI.
  • Biofilms protect the pathogenic organism from antimicrobials and host defense mechanisms.
  • Urinary stasis due to drainage failure and contamination of the urine collection bag can result in ascending infections.
  • Urinary catheterization disrupts host defense mechanisms and provides access of uropathogens to the urinary system.

Predictive/risk factors for CAUTI


Duration of catheterization is one of the most significant risk factors in the development of CAUTI.



  • Placement of urinary catheter for inappropriate indications.
  • Repeated catheterization.
  • Improper sterile technique with catheter placement.
  • Failure to maintain a closed drainage system.
  • Prolonged urinary catheterization.
  • Advanced age.
  • Female gender.
  • Impaired immunity.
  • Diabetes mellitus.

Prevention



  • Alternative methods to internal urinary catheters such as intermittent catheterization or external catheters.
  • Perform and maintain sterile technique with internal urinary catheter placement.
  • Maintain a closed drainage system with unobstructed urine flow.
  • The use of antiseptic impregnated urinary catheters may be considered.
  • Prompt removal of internal urinary catheters when no longer indicated.

Diagnosis


Typical presentation


Unexplained fever, leukocytosis, and decompensation in a patient with indwelling urinary catheter, especially if prolonged, should trigger evaluation of a possible CAUTI.


Clinical diagnosis


History

Prolonged internal urinary catheterization in the presence of symptoms such as fever, chills, and rigors.


Physical examination

Visible erythema, tenderness, and purulent discharge from the urethral meatus, as well as purulent urine in the catheter collecting system suggest the urinary catheter as a source of infection.


Laboratory diagnosis


List of diagnostic tests


  • Specimens for urine culture should only be collected when CAUTI is suspected based on abnormal urinalysis.
  • Urine culture should be collected after removing the indwelling catheter and obtaining a midstream specimen.
  • If the catheter cannot be removed, specimens for urine culture should be collected through a catheter port using aseptic technique.
  • In patients with long‐term indwelling catheters, it is recommended that a new indwelling urinary catheter be placed prior to specimen collection for urine cultures.
  • Urine culture specimens should not be obtained from the urinary collecting bag.

List of imaging techniques


  • Ultrasound and/or CT scan of the kidneys may be considered in patients with CAUTI who present with clinical findings of acute pyelonephritis.

Potential pitfalls/common errors made regarding diagnosis of disease


  • Failure to implement or adhere to daily CAUTI prevention bundle adherence measures.
  • Lack of aseptic technique in the collection of urine specimen may result in contamination and false positive cultures.

Treatment



  • Prompt removal of indwelling urinary catheters.
  • Empiric coverage for Gram‐negative organisms is recommended until cultures are available.
  • Duration of antibiotic treatment is dependent on the patient’s response.

Prognosis


Mortality attributed to CAUTI is approximately 2.3% and is likely to be influenced by the underlying acute illness and comorbidities.


Follow‐up tests and monitoring


All patients diagnosed with hospital‐acquired infection should be closely monitored for clinical response to treatment.


Ventilator‐associated event and ventilator‐associated pneumonia


Background


Definition of disease



  • VAE is defined as worsening oxygenation following ≥2 days of stable or decreasing FiO2 or PEEP. There are three tiers within the VAE algorithm:

    • Ventilator‐associated condition (VAC): increase in daily FiO2 ≥20% over daily minimum FiO2 sustained for ≥2 days or increase in PEEP of ≥3 over daily minimum PEEP for ≥2 days.
    • Infection‐related ventilator‐associated complication (IVAC): ≥3 days of mechanical ventilation and within 2 days of worsening oxygenation, the patient develops a temperature >38°C or <36°C, or WBC ≥12 000 or ≤4000 and a new antibiotic is started and continued for ≥4 days.

  • Possible or probable ventilator‐associated pneumonia (VAP): above criteria for IVAC plus positive bacterial laboratory confirmation or lung histopathology.

Etiology


Predominant organisms are:



  • P. aeruginosa.
  • S. aureus.
  • Klebsiella pneumoniae.
  • Acinetobacter species.
  • E. coli.

Pathology/pathogenesis



  • Microaspiration of oropharyngeal contents and migration of bacteria around the endotracheal tube cuff is the primary method by which bacteria invade the lower respiratory tract.
  • Intubation procedure can introduce pathogenic organisms resulting in infection.
  • Colonization of the endotracheal tube or the ventilator circuit by bacteria with the formation of biofilm.
  • Natural host defense mechanism of secretion clearance is disrupted by the presence of an endotracheal tube and sedation.

Predictive/risk factors



  • Skill of the operator performing endotracheal intubation.
  • Prolonged mechanical ventilation.
  • Reintubation.
  • Position of endotracheal and gastric tubes. Orotracheal intubation and orogastric tubes are preferred over nasotracheal intubation and nasogastric tubes to reduce the risk of VAP.
  • Risk factors for MDR organisms:

    • Antibiotic therapy in previous 90 days.
    • Current hospitalization of 2 days or more.
    • High frequency of antibiotic resistance in the community or hospital.
    • Residence in nursing home.
    • Home infusion therapy.
    • Chronic dialysis.
    • Home wound care.
    • Family member with multidrug‐resistant organism.
    • Immunosuppressive disease and/or therapy.

Prevention



  • Non‐invasive ventilation in selected patients to prevent intubation.
  • Maintain semi‐recumbent position of 30–45° to prevent aspiration.
  • Oral chlorhexidine to prevent oropharyngeal colonization.
  • Continuous aspiration of subglottic secretions can reduce the risk of VAP.
  • Endotracheal tube cuff pressure should be maintained >20 cmH2O to prevent leakage of secretions around the cuff into the lower respiratory tract.
  • Remove contaminated condensate from the ventilator circuit and prevent condensate from entering the endotracheal tube.
  • Reduce the duration of mechanical ventilation and accelerate weaning through adherence to daily ventilator bundle measures.

Diagnosis


Differential diagnosis



















Differential diagnosis Features
Pulmonary embolism (PE) Risk factors for PE
No purulent secretions
Negative cultures
CT angiogram or V/Q scan showing PE
Congestive heart failure Non‐purulent secretions
Reduced ventricular function on echocardiogram
Improvement with diuretics
No response to antibiotics
Pulmonary hemorrhage Bloody secretions
No response to antibiotics
Bronchoscopy with hemorrhagic lavage
Atelectasis No purulent secretions
No response to antibiotics
Fleeting opacities on imaging

Typical presentation


Increase in purulent secretions, fever, and worsening hypoxemia suggest VAP.


Clinical diagnosis


Physical examination


  • Auscultation for the presence of crackles, wheezing, and/or egophony.
  • Dullness to percussion may indicate consolidated lung or the presence of a pleural effusion.
  • Daily assessment of the quality and quantity of endotracheal tube secretions

Laboratory diagnosis


List of diagnostic tests


  • Lower respiratory tract secretions should be sent for culture.

    • Bronchoscopic specimen collection may be considered.

  • Blood cultures should be collected prior to administration of antibiotics.
  • A diagnostic thoracentesis should be performed if a patient has a moderate or large pleural effusion to rule out parapneumonic effusion or empyema.

List of imaging techniques


  • Chest radiography should be performed in patients with suspected VAP to:

    • Define severity of pneumonia.
    • Identify presence of complications such as effusion or cavitation.

  • Chest ultrasonography may be obtained in institutions with appropriate ultrasound expertise.

Potential pitfalls/common errors made regarding diagnosis of disease



  • Failure to maintain accurate duration dates for mechanical ventilation.
  • Failure to implement or fully adhere to daily ventilator bundle measures.
  • Lack of proper technique in the collection of tracheal aspirate or bronchoscopic specimen may result in contamination and/or inadequate specimen.

Treatment



  • Antibiotic therapy is recommended in patients with no known risk factors for MDR pathogens (Table 44.1).
  • Combination antibiotic therapy is recommended in patients with suspected MDR pathogens (Table 44.2).
  • Duration of appropriate antibiotic treatment for VAP in a patient with appropriate clinical response is 7 days.
  • P. aeruginosa should be treated for at least 14 days.
  • Aerosolized antibiotics may be considered as adjunctive therapy in patients with VAP due to MDR Gram‐negative pathogens not responding to intravenous therapy.

Prognosis


Mortality attributed to VAP has been reported prior to the new VAE definition to be approximately 13% and is likely to be influenced by the underlying acute illness and comorbidities.


Table 44.1 Initial empiric antibiotic therapy for suspected VAP in patients with no known risk factors for MDR pathogens.













Suspected pathogen Recommended empiric antibiotic
Streptococcus pneumoniae
Haemophilus influenzae
MRSA
Ceftriaxone
Or
Levofloxacin/moxifloxacin
Sensitive enteric Gram‐negative bacilli:

  • E. coli
  • Proteus
  • K. pneumoniae
  • Serratia
  • Enterobacter
Ampicillin/sulbactam

Table 44.2 Initial empiric antibiotic therapy for suspected VAP in patients with risk factors for MDR pathogens.










Suspected MDR pathogen Recommended combination antibiotic therapy
Pseudomonas aeruginosa
Klebsiella pneumoniae
Acinetobacter species
Methicillin‐resistant Staphylococcus aureus (MRSA)
Antipseudomonal cephalosporin
Or
Antipseudomonal carbapenem
Or
Antipseudomonal β‐lactam/β‐lactamase inhibitor (piperacillin/tazobactam)
Plus
Vancomycin or linezolid

Clostridium difficile infection


Background


Definition of disease



  • CDI is one of the main causes of antibiotic‐associated diarrhea in hospitalized patients. Diagnosis is based on a combination of clinical and laboratory findings in patients with current or recent health care exposure.
  • The most common clinical finding is diarrhea:

    • ≥3 unformed stools within a 24 hour period.
    • The Bristol stool scale can be used in the initial assessment: ≥3 stools is categorized as type 5 or greater within 48 hours or 1 stool is categorized as type 7 (watery) within the past 24 hours.

  • Laboratory confirmation with either a positive test on an unformed stool specimen for toxin‐producing C. difficile or direct colonoscopic visualization with findings revealing pseudomembranous colitis.

Etiology


Clostridium difficile is an anaerobic organism responsible for the majority of cases of antibiotic‐associated colitis.


Pathology/pathogenesis



  • CDI is the result of person‐to‐person spread through the fecal–oral route. The most important mechanism by which C. difficile is spread is through the hands of health care workers contaminated with C. difficile spores.
  • Antimicrobial therapy results in alteration of the normal intestinal flora, predisposing patients to the development of C. difficile colitis.
  • Pathogenic C. difficile produces two distinct toxins. Toxin A is an enterotoxin and toxin B is a cytotoxin. Both toxins bind to the intestinal mucosal cells resulting in mucosal inflammation and the development of pseudomembranous colitis. This mucosal inflammation leads to diarrhea (bloody or non‐bloody), and in severe cases, ileus with toxic megacolon.
  • NAP1 is a hypervirulent strain of C. difficile most commonly associated with severe and fulminant colitis.
  • Asymptomatic C. difficile colonization is common, with an estimated prevalence of 7–26% in acute care facilities.

Predictive/risk factors



  • Inappropriate use of antibiotics. Any antibiotic can predispose to CDI. The most frequently implicated antibiotics include clindamycin, fluoroquinolones, and cephalosporins.
  • Hospitalization.
  • Advanced age >70 years.
  • Severe illness and impaired immunity:

    • Chemotherapy.
    • Hematopoietic stem cell transplant.
    • Gastrointestinal surgery.

  • Use of proton pump inhibitors.
  • Failure to utilize appropriate contact precautions and disposable medical devices, as well as improper hand hygiene.
  • Improper sterilization of rooms and equipment after exposure.

Prevention


Screening



  • Stool culture, enzyme immunoassay (EIA) for C. difficile toxin, or PCR of liquid stool sample in patients with risk factors and new onset diarrhea.

Primary prevention



  • Antibiotic stewardship. Optimize the use and duration of antibiotic therapy to minimize unnecessary antibiotic exposure.
  • Early detection and contact isolation precautions:

    • Use of private rooms is recommended.
    • Gloves and gowns should be worn upon room entry and removed prior to exiting the room.
    • Strict adherence to hand hygiene with conventional soap and water. Instruct visitors on the necessity of hand hygiene.
    • Dedicated disposable medical equipment should be utilized.
    • Contact precautions should be maintained for the duration of diarrhea.

  • Environmental cleansing with chlorine‐based agents is recommended.

Secondary prevention



  • Antimicrobial therapy:

    • Prolonged course of oral vancomycin with a gradual taper in recurrent disease.

  • Fidaxomicin may be considered for recurrent disease.
  • Fecal microbiota therapy (FMT):

    • Indications:

      • Recurrent or relapsing infection:

        • ≥3 episodes of mild–moderate CDI and failure of 6–8 week vancomycin taper.
        • ≥2 episodes of severe CDI.

      • Persistent moderate (>1 week) or severe (>48 hours) CDI not responding to appropriate therapy.
      • Protracted CDI:

        • ≥3 weeks of ongoing symptoms on appropriate antimicrobial therapy.

      • Absolute contraindications to FMT:

        • Decompensated liver cirrhosis.
        • HIV/AIDS.
        • Bone marrow transplant recipients.
        • Severe immunodeficiency.
        • Anaphylactic food allergy which was not excluded from donor diet.

      • FMT may be delivered by colonoscopy or flexible sigmoidoscopy.
      • Repeat FMT may be considered if inadequate response to initial FMT therapy.

Diagnosis


Differential diagnosis
















Differential diagnosis Features
Acalculous cholecystitis Right upper quadrant (RUQ) tenderness
Hepatic function panel with cholestatic profile
RUQ ultrasound or HIDA scan showing cholecystitis
Infectious diarrhea (not due to C. difficile) Negative C. difficile testing
Stool culture positive for other organism
May have bloody or non‐bloody diarrhea
No significant antibiotic exposure or recent hospitalization
Ischemic colitis Patient risk factors for ischemia
Acute onset
No significant antibiotic exposure or recent hospitalization
May have bloody or non‐bloody diarrhea
Elevated lactate
Negative C. difficile testing

In CDI, diarrhea (mucus, bloody, or non‐bloody) remains the most common clinical presentation, especially in the setting of antibiotic use or recurrent hospitalization. Ileus due to CDI may present as abdominal pain and distension without associated diarrhea.


Clinical diagnosis


History


  • Patient reports of bloody or non‐bloody diarrhea with recent hospitalization, antibiotic exposure, or contact with an individual known to have C. difficile should raise awareness regarding possible CDI.

Physical examination


  • Observation for bloody or mucus/non‐bloody diarrhea. Auscultation for bowel sounds should be performed to assess for ileus. Examination and palpation of the abdomen for distension and tenderness to evaluate for progression to ileus and megacolon.

Disease severity classification


  • Mild to moderate:

    • White blood cell count <15 000/mm3.
    • Serum creatinine <1.5 times baseline.

  • Severe:

    • White blood cell count ≥15 000/mm3.
    • Serum creatinine ≥1.5 times baseline.

  • Severe and complicated:

    • White blood cell count ≥15 000/mm3.
    • Serum creatinine ≥1.5 times baseline.
    • Hypotension or shock.
    • Ileus or megacolon.

Laboratory diagnosis


List of diagnostic tests


  • Testing for C. difficile should be performed only on unformed stool, unless ileus from C. difficile is suspected.
  • Stool culture is the most sensitive test to detect CDI. It is limited by a slow turnaround time.
  • EIA testing for C. difficile toxins A and B is rapid, but is less sensitive than stool culture.
  • PCR testing is rapid, sensitive, and specific.
  • Two‐step testing may be considered to increase diagnostic accuracy.
  • Colonoscopy with biopsy may be performed to identify pseudomembranous colitis.

List of imaging techniques


  • Abdominal radiography (X‐ray or CT scan) should be obtained if complications of CDI such as ileus, megacolon, or perforation are suspected.

Potential pitfalls/common errors made regarding diagnosis of disease



  • Lack of consideration for CDI. Delay in testing and diagnosis can result in significant delay in treatment and spread of infection.
  • CDI is a clinical diagnosis with confirmatory laboratory findings. Sending C. difficile stool specimens without appropriate clinical symptoms may result in identification of C. difficile carrier state, which does not require treatment.

Treatment



  • CDI is characterized as non‐severe, severe, fulminant or recurrent.
  • A surgical consultation should be obtained in patients with severe CDI.











Clinical definition Clinical data Treatment


  • Initial episode, non‐severe disease
  • Inital episode, severe
  • Inital episode, fulminant
  • First recurrence
  • Second recurrence



  • WBC < 15 000/mm3 and serum creatinine level < 1.5 times baseline
  • WBC ≥ 15 000/mm3 or serum creatinine level ≥ 1.5 times baseline
  • Hypotension or shock, ileus, megacolon



  • Oral vancomycin 125 mg four times per day or oral fidaxomicin 200 mg twice daily, 10 days
  • Oral vancomycin 125 mg four times per day or oral fidaxomicin 200 mg twice daily, 10 days
  • Oral vancomycin 500 mg four times per day, plus intravenous metronidazole 500 mg every 8 hours. If ileus, consider adding rectal vancomycin
  • Same as initial treatment
  • Vancomycin in tapered or pulsed regimen

Prognosis



  • Mortality attributed to health care‐associated CDI ranges from 6% to 30%.
  • Infection with hypervirulent strain NAP1/BI/027 may result in more severe disease and higher mortality.

Natural history of untreated disease



  • The course of untreated CDI is dependent on the severity of disease, strain of C. difficile, and the underlying immune function of the patient.
  • Untreated patients may have increasingly voluminous diarrhea, develop ileus, and progress to toxic megacolon with potential perforation and development of an overwhelming septic state.

Follow‐up tests and monitoring



  • Repeat testing during the same episodes of diarrhea is not recommended.
  • Test of cure following treatment of C. difficile is not recommended.

Pressure ulcer infection


Background


Definition of disease



  • A laboratory confirmed superficial or deep skin or soft tissue infection with at least two of the following signs or symptoms with identifiable risk factor(s): erythema, edema, or tenderness of the wound edges.

    • Plus, organisms identified from tissue biopsy or aspiration of fluid from the ulcer margin.

Etiology


Predominant organisms are:



  • Enterobacter species.
  • Staphylococci.
  • Enterococcus faecalis.

Pathology/pathogenesis



  • Pressure ulcers develop due to localized injury to the skin and/or soft tissue. These injuries typically occur over bony prominences as a result of sustained pressure and/or friction.
  • Breakdown of the skin barrier from a combination of pressure, friction, shearing forces, and moisture predisposes to bacterial colonization and the development of skin and soft tissue infections.
  • Externally applied pressure on body surfaces exceeds the capillary perfusion pressure within the tissue. This disrupts the microcirculation resulting in inflammation, free radical generation, and hypoxic tissue necrosis.

Predictive/risk factors



  • Immobility.
  • Malnutrition.
  • Reduced perfusion:

    • Peripheral arterial disease.
    • Congestive heart failure.

  • Sensory loss:

    • Spinal cord injury.
    • Neuropathy.

  • Moisture.

Prevention


Screening


Risk assessment and a complete skin assessment should be conducted on all patients admitted to the ICU and repeated as required based on risk factors and patient acuity.


Primary prevention



  • Cushion dressings should be applied to areas of high risk to protect the skin.
  • Daily skin inspection.
  • Frequent repositioning of immobile, bedbound patients with maintenance of dry skin environment.

Diagnosis


Typical presentation


Pressure ulcer infections typically present with erythema, edema, and tenderness with or without purulent discharge, on an area of the body vulnerable to pressure ulcers.


Clinical diagnosis


History

Prolonged immobility and infectious symptoms should raise concern for pressure ulcer infection.


Physical examination

Daily assessment of pressure ulcers for depth, visible erythema, edema, purulent discharge, or visible bone.


Disease severity classification

Pressure ulcers are categorized into stages:



  • Stage I: non‐blanchable erythema with intact skin.
  • Stage II: partial thickness loss of dermis with red‐pink wound bed.
  • Stage III: full thickness skin loss. Subcutaneous fat may be visible in areas of adipose tissue.
  • Stage IV: full thickness tissue loss with exposed tendon, muscle, and/or bone.
  • Unstageable: full thickness skin or tissue loss with depth unknown.

Laboratory diagnosis



  • Cultures should be collected either by tissue biopsy or aspirate of fluid at the ulcer margin.
  • MRI, CT scan, and/or bone scans are recommended in patients with infected pressure ulcers with high clinical suspicion for osteomyelitis.

Potential pitfalls/common errors made regarding diagnosis of disease



  • Failure to perform a thorough daily skin assessment in patients at high risk for pressure ulcers or with existing pressure ulcers

Treatment



  • Pain control.
  • Local wound care.
  • Consultation of wound care professional.
  • Intravenous antibiotics.
  • Patients with pressure ulcer infections and evidence of tissue necrosis should have surgical consultation and debridement.

Prognosis


Natural history of untreated disease



  • Neglected pressure ulcers will progress in severity.
  • Bone involvement may result in osteomyelitis. Secondary bacteremia may develop and can progress to a potentially lethal septic state.

Follow‐up tests and monitoring



  • Patients treated for pressure ulcer infections should have frequent skin examinations to ensure appropriate healing.

Reading list



  1. Dudeck MA, et al. National Healthcare Safety Network report, data summary for 2013, device‐associated module. Am J Infect Control 2015; 43(3):206–21.
  2. Yokoe DS, et al. A compendium of strategies to prevent healthcare‐associated infections in acute care hospitals: 2014 updates. Infect Control Hosp Epidemiol 2014; 35(8):967–77.
  3. Zimlichman E, et al. Health care‐associated infections. A meta‐analysis of costs and financial impact on the US health care system. JAMA Intern Med 2013; 173(22):2039–46.

Suggested websites


www.cdc.gov/drugresistance/


www.cdc.gov/hai/


www.cdc.gov/nhsn/


www.idsociety.org/IDSA_Practice:Guidelines/


www.npuap.org/


Guidelines


National society guidelines
































Title Source Date and reference/weblink
Guidelines for the Prevention of Intravascular Catheter‐Related Infections Centers for Disease Control and Prevention (CDC) 2011
www.cdc.gov/infectioncontrol/guidelines/BSI/index.html
Strategies to Prevent Catheter‐Associated Urinary Tract Infections in Acute Care Hospitals: 2014 Update IDSA 2014
Lo E, et al. Infect Control Hosp Epidemiol 2014;35(5):464–79
Guidelines for the Management of Adults with Hospital‐Acquired, Ventilator‐Associated, and Healthcare‐Associated Pneumonia American Thoracic Society (ATS) and IDSA 2005
ATS; IDSA. Am J Respir Crit Care Med 2005;171:388–416
Strategies to Prevent Ventilator‐Associated Pneumonia in Acute Care Hospitals Society for Healthcare Epidemiology of America (SHEA) and IDSA 2008
Coffin SE, et al. Infect Control Hosp Epidemiol 2008;29:S31–40
Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children: 2017 Update SHEA and IDSA 2018
McDonald LC, et al. Clin Infect Dis 2018;66(7):e1–48
Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline National Pressure Injury Advisory Panel (NPUAP), EPUAP, and PPPIA 2014
www.npuap.org/
Nov 20, 2022 | Posted by in ANESTHESIA | Comments Off on 44: Infections Acquired in the Intensive Care Unit
Premium Wordpress Themes by UFO Themes